Inhibitary Effects Of Melatonin On The Proliferation Of E₂-induced Rat Pituitary Prolactin-secreting Tumor And The Mechanisms Of Cellular Biology

In present study, the effects of melatonin (MLT) on the proliferation of 17-β-estradiol (E2)-induced pituitary prolactin-secreting tumor (prolactinoma) of the rats and the mechanisms of cellular biology in vivo and in vitro were investigated. To combine our previous findings of the pathogenesis of prolactinoma, we focused mainly on the cell biology mechanisms of oncostatic effects of MLT on prolactinoma, such as the induction of the apoptosis pathway in vivo and in vitro, and the inhibitory effects on the energy metabolism. In order to provide an essential experimental basic for the utilization of MLT on the clinical practice, and new pathway for the therapy of prolactinoma, the effects of MLT on the proliferation and the apoptosis of E2-induced pituitary prolactin-secreting tumor (prolactinoma) in vitro and in vivo were investigated in part I and part II. It was found that MLT inhibited cells proliferation of prolactinoma and increased the apoptosis of prolactinoma. The principal mechanism may realated with promoting the caspase-3 activity and Bax expression, decreasing the expression of Bcl-2, decreasing mitochondrial membrane stability and promoting the release of cytochrome c. As the main site of energy production and deposition in the mitochondria, we investigated the effect of MLT on the activities of the four complexes of the respiratory chain in part III. The data indicated that MLT obviously inhibited the activities of the four complexes in the respiratory chain and the ATP production of prolactinoma.